Showing papers on "Salidroside published in 2014"

Anticancer effect of salidroside on A549 lung cancer cells through inhibition of oxidative stress and phospho-p38 expression.

Abstract: Oxidative stress is important in carcinogenesis and metastasis. Salidroside, a phenylpropanoid glycoside isolated from Rhodiola rosea L., shows potent antioxidant properties. The aim of the present study was to investigate the roles of salidroside in cell proliferation, the cell cycle, apoptosis, invasion and epithelial-mesenchymal transition (EMT) in A549 cells. The human alveolar adenocarcinoma cell line, A549, was incubated with various concentrations of salidroside (0, 1, 5, 10 and 20 μg/ml) and cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Propidium iodide (PI) staining was used to determine the cell cycle by flow cytometry. Cell apoptosis was detected by Annexin V-fluorescein isothiocyanate and PI double-staining, and tumor invasion was detected by Boyden chamber invasion assay. Western blot analysis was performed to detect the expression of EMT markers, Snail and phospho-p38. The results showed that salidroside significantly reduced the proliferation of A549 cells, inhibited cell cycle arrest in the G0/G1 phase and induced apoptosis. Salidroside inhibited transforming growth factor-β-induced tumor invasion and suppressed the protein expression of Snail. As an antioxidant, salidroside inhibited the intracellular reactive oxygen species (ROS) formation in a dose-dependent manner in A549 cells, and depletion of intracellular ROS by vitamin C suppressed apoptosis by salidroside treatment. Salidroside was also found to inhibit the expression of phospho-p38 in A549 cells. In conclusion, salidroside inhibits cell proliferation, the cell cycle and metastasis and induces apoptosis, which may be due to its interference in the intracellular ROS generation, thereby, downregulating the ROS-phospho-p38 signaling pathway.

Rhodiola rosea in vitro culture - phytochemical analysis and antioxidant action

Abstract: Various Rhodiola rosea organs and tissues from in vitro culture were studied in two areas: searching for the biological active four phenolic compounds and measurement of antioxidant activity of dry residues of EtOH-extracts soluble in PBS using chemiluminescence method. For phytochemical investigation HPLC method was used. Salidroside was typical for organs of intact plant, rosavin for roots of different origin and shoots of intact plants, triandrin was more typical for tissue cultured in vitro, but it was found in all studied samples. Caffeic acid was detected mainly in green and yellow lines of callus, less in other Rhodiola rosea plant material. The highest antioxidant activity showed the extract from 1,5-years-old callus of green and yellow line, which contained caffeic acid and triandrin. Further observations are in progress.

Antidepressant-like effects of salidroside on olfactory bulbectomy-induced pro-inflammatory cytokine production and hyperactivity of HPA axis in rats

Abstract: Salidroside (SA) is the primary bioactive marker compound in the standardized extracts from Rhodiola rosea. Although it has potential antidepressant activity in a rat behavioral despair model, the mechanisms of antidepressant effect for SA remain unclear. The objective of this study was to evaluate the antidepressant effects of SA and to discuss the potential mechanisms in olfactory bulbectomized (OBX) rats. SA of 20, 40 mg/kg (p.o.) for 2 weeks notably alleviated OBX-induced hyperactivity in open field test, decreased immobility time in TST and FST. Chronic treatment with SA could remarkably reduce TNF-α and IL-1β levels in hippocampus. Western blot showed that SA could markedly increase glucocorticoid receptor (GR) and brain-derived neurotrophic factor (BDNF) expression in the hippocampus. Besides, SA could also attenuate corticotropin-releasing hormone (CRH) expression in hypothalamus, as well as reducing significantly the levels of serum corticosterone. In conclusion, this study demonstrated that OBX rats treated with SA could significantly improve the depressive-like behaviors. The antidepressant mechanisms of SA might be associated with its anti-inflammatory effects and the regulation of HPA axis activity. Reversal of abnormalities of GR may be partly responsible for those effects. These findings suggested that SA might become a beneficial agent to prevent and treat the depression.

Salidroside Protects Caenorhabditis elegans Neurons from Polyglutamine-Mediated Toxicity by Reducing Oxidative Stress

Abstract: Polyglutamine (polyQ) aggregation plays a pivotal role in the pathological process of Huntington’s disease and other polyQ disorders. Therefore, strategies aiming at restoring dysfunction and reducing stresses mediated by polyQ toxicity are of therapeutic interest for proteotoxicity diseases. Salidroside, a glycoside from Rhodiola rosea, has been shown to have a variety of bioactivities, including antioxidant activity. Using transgenic Caenorhabditis elegans models, we show here that salidroside is able to reduce neuronal death and behavioral dysfunction mediated by polyQ expressed in ASH neurons, but the neuroprotective effect is not associated with prevention of polyQ aggregation per se. Further experiments reveal that the neuroprotective effect of salidroside in C. elegans models involves its antioxidant capabilities, including decrease of ROS levels and paraquat-induced mortality, increase of antioxidant enzyme activities and reduction of lipid peroxidation. These results demonstrate that salidroside exerts its neuroprotective function against polyQ toxicity via oxidative stress pathways.

Inhibition of xanthine oxidase by Rhodiola crenulata extracts and their phytochemicals.

Abstract: Using a fractionation technique, four phytochemicals were isolated from Rhodiola crenulata extracts. These compounds were identified as 4'-hydroxyacetophenone (4-HAP), epicatechin-(4β,8)-epicatechin gallate (B2-3'-O-gallate), salidroside, and p-tyrosol using mass spectrometry and nuclear magnetic resonance spectroscopy. The inhibition of xanthine oxidase (XO) activity by these purified compounds was then evaluated and compared to that of a known XO inhibitor (allopurinol; IC50 = 12.21 ± 0.27 μM). Both 4-HAP and B2-3'-O-gallate showed an XO inhibitory effect, for which the half maximal inhibitory concentration (IC50) values were 15.62 ± 1.19 and 24.24 ± 1.80 μM, respectively. However, salidroside and p-tyrosol did not show significant inhibitory effects on XO at 30 μM. Furthermore, an inhibition kinetics study indicated that 4-HAP and B2-3'-O-gallate are mixed competitive inhibitors. The inhibition constants (Ki) of 4-HAP and B2-3'-O-gallate were 8.41 ± 1.03 and 6.16 ± 1.56 μM, respectively. These results suggest that 4-HAP and B2-3'-O-gallate are potent XO inhibitors.

Effects of Salidroside on Cobalt Chloride-Induced Hypoxia Damage and mTOR Signaling Repression in PC12 Cells

Abstract: Salidroside (SA), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has been documented to exert a broad spectrum of pharmacological properties, including protective effects against neuronal death induced by various stresses. To provide further insights into the neuroprotective functions of SA, this study examined whether SA can attenuate cobalt chloride (CoCl2)-induced hypoxia damage and mammalian target of rapamycin (mTOR) signaling repression in PC12 differentiated cells. Differentiated PC12 cells were exposed to CoCl2 for 12 h to mimic hypoxic/ischemic conditions and treated with SA at the same time, followed by electron microscopy and analysis of cell viability, intracellular reactive oxygen species (ROS) level, hypoxia-inducible factor-1α (HIF-1α) level, and the regulated in development and DNA damage responses (REDD1)/mTOR/ p70 ribosomal S6 kinase (p70S6K) signaling pathway. Our data indicated that SA can dramatically attenuate the ultrastructural damage of mitochondria induced by CoCl2 and significantly decrease CoCl2-induced ROS production. Moreover, phosphorylated mammalian target of rapamycin (p-mTOR) was significantly reduced by CoCl2, and this inhibition was relieved by the treatment of SA in PC12 cells, as evidenced by immunoblot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analyses. The SA effects were blocked by pretreatment of RAD001. The results indicate that SA can rescue CoCl2-induced repression of REDD1/mTOR/ p70S6K signal transduction in PC12 cells. Our data demonstrate that SA is able to attenuate CoCl2-induced hypoxia damage and mTOR signaling repression, suggesting that SA may protect brain neurons from ischemic injury through mTOR signaling, and provide new insights into the prevention and treatment of cerebral ischemic.

The metabolism of salidroside to its aglycone p-tyrosol in rats following the administration of salidroside.

Abstract: Salidroside is one of the major phenolic glycosides in Rhodiola, which has been reported to possess various biological activities. In the present study the in vivo deglycosylation metabolism of salidroside was investigated and its aglycone p-tyrosol but not the original salidroside was identified as the main form in rat tissues following the administration of salidroside. After the i.v. administration of salidroside at a dose of 50 mg/kg in rats, salidroside was quantified only in the liver, kidney and heart tissues. The highest level of p-tyrosol was detected in the heart, followed by the spleen, kidney, liver and lungs, in order. Salidroside was detected only in the liver, in contrast, p-tyrosol was detectable in most tissues except the brain, and the kidney tissues contained a significant amount of p-tyrosol compared to the other tissues after the i.g. administration of 100 mg/kg salidroside. The excretion behaviour revealed that the administrated salidroside mainly eliminated in the form of salidroside but not its aglycone metabolite p-tyrosol through urine. After i.v. and i.g. administration in rats, 64.00% and 23.80% of the total dose was excreted through urine in the form of salidroside, respectively. In addition, 0.19% and 2.25% of the dose was excreted in the form of p-tyrosol through urine after i.v. and i.g. administration, respectively. The faecal salidroside and p-tyrosol concentrations were 0.3% and 1.48% of the total dose after i.v. administration, respectively. After the i.g. administration of salidroside, trace salidroside and p-tyrosol were quantified in faeces within 72 h. In addition, the biliary excretion levels of salidroside after i.v. and i.g. administration were 2.86% and 0.02% of the dose, respectively. The obtained results show that salidroside was extensively metabolised to its aglycone p-tyrosol and distributed to various organs and the orginal salidroside was cleared rapidly through urine following the administration of salidroside.

Sequential release of salidroside and paeonol from a nanosphere-hydrogel system inhibits ultraviolet B-induced melanogenesis in guinea pig skin.

Abstract: Melanin is the one of most important pigments for skin color in mammals. Excessive biosynthesis of melanin induces various pigment disorders. Much effort has been made to develop regulators to minimize skin pigmentation abnormalities. However, only a few of them are used, primarily because of safety concerns and low efficiency. In this study, we aimed to construct a novel nanosphere-gel for sequential delivery of salidroside and paeonol, to investigate the synergistic effects of these drugs in anti-melanogenesis, and to decrease their potential for toxicity in high dosage. Nanospheres were prepared and characterized for their particle size, polydispersity index, zeta potential, and morphological properties. The optimized nanospheres were incorporated in carbomer hydrogel with both paeonol and salidroside entrapped to form a dual drug-releasing nanosphere-gel. With this nanosphere-gel, rapid release of salidroside from the hydrogel followed by sustained release of paeonol from the nanosphere was achieved. Using a classical model of the melanogenesis response to ultraviolet exposure, it was shown that the anti-melanogenesis effects of the dual drug-releasing system, in which the doses of the individual drugs were decreased by half, was obviously enhanced when compared with the effects of the single drug preparations. Mechanistically, the burst release of salidroside from the hydrogel may enable prompt suppression of melanocyte proliferation on exposure to ultraviolet B radiation, while the paeonol released in a sustained manner can provide continuous inhibition of tyrosinase activity in melanocytes. Combined delivery of salidroside and paeonol was demonstrated to be a promising strategy for enhancing the therapeutic efficacy of these agents in anti-melanogenesis and reducing their toxicity, so may have great potential in nanomedicine.

Amphiphilic Chitosan Derivatives-Based Liposomes: Synthesis, Development, and Properties as a Carrier for Sustained Release of Salidroside

Abstract: A novel amphiphilic chitosan derivative of N,N-dimethylhexadecyl carboxymethyl chitosan (DCMCs) was synthesized. The structure of DCMCs was confirmed via FT-IR and 1H NMR, and the critical micelle concentration (CMC) was investigated by fluorescence spectroscopy. The results indicated that DCMCs has hydrophilic carboxyl and hydrophobic methylene groups and the CMC value was 23.00 mg·L–1. The polymeric liposomes (DCMCs/cholesterol liposomes, DC-Ls) were developed, and its properties were evaluated. The DC-Ls exhibited multilamellar spheres with positive charge (+73.30 mV), narrow size distribution (PDI = 0.277), and good crystal properties. Salidroside was first to encapsulate into DC-Ls. Compared with traditional liposomes (phosphatidylcholine/cholesterol liposome, PC-Ls), DC-Ls showed higher encapsulation efficiency (82.46%) and slower sustained release rate. The in vitro salidroside release from DC-Ls was governed by two distinct stages (i.e., burst release and sustained release) and was dependent on th...

Salidroside attenuates concanavalin A-induced hepatitis via modulating cytokines secretion and lymphocyte migration in mice.

Abstract: Salidroside, isolated from the medicinal plant Rhodiola, was reported to serve as an “adaptogen.” This study was designed to explore the protective effect of salidroside on concanavalin A- (Con A-) induced hepatitis in mice and investigate potential mechanisms. C57BL/6 mice were randomly divided into control group, Con A group, and salidroside group. Salidroside (50 mg/kg) was injected intravenously followed by Con A administration. The levels of ALT, AST, inflammatory cytokines and CXCL-10 were examined. The pathological damage of livers was assessed, the amounts of phosphorylated IκBα and p65 were measured, and the numbers of CD4+ and CD8+ T lymphocytes in the blood, spleen and infiltrated in the liver were calculated. Our results showed that salidroside pretreatment reduced the levels of ALT, AST dramatically and suppressed the secretion of proinflammatory cytokines through downregulating the activity of NF-κB partly. Salidroside altered the distribution of CD4+ and CD8+ T lymphocyte in the liver and spleen through regulating CXCL-10 and decreased the severity of liver injuries. In conclusion, these results confirm the efficacy of salidroside in the prevention of immune mediated hepatitis in mice.

Binding to WGR Domain by Salidroside Activates PARP1 and Protects Hematopoietic Stem Cells from Oxidative Stress

Abstract: Aims: A component of the base excision repair pathway, poly(ADP-ribose) polymerase-1 (PARP1) functions in multiple cellular processes, including DNA repair and programmed cell death. We previously showed that Salidroside, a phenylpropanoid glycoside isolated from medicinal plants, prevented the loss of hematopoietic stem cells (HSCs) in native mice and rescued HSCs repopulating in transplanted recipients under oxidative stress. The aim of this study was to investigate the mechanism by which PARP1 activation by Salidroside maintains HSCs under oxidative stress. Results: We found that although there were no spontaneous defects in hematopoiesis in Parp1−/− mice, oxidative stress compromised the repopulating capacity of Parp1−/− HSCs in transplanted recipient mice. A biochemical study using truncated proteins lacking the defined functional domains of PARP1 showed that the tryptophan-glycine–arginine-rich (WGR) domain of PARP1 was critical for Salidroside binding and subsequent PARP1 activation under oxidative stress. Functionally, complementation of Parp1−/− HSCs with full-length PARP1WT, but not the PARP1R591K mutant in WGR domain restored Salidroside-stimulated PARP1 activation in vitro. Mechanistically, activated PARP1 by Salidroside enhanced the repopulating capacity of the stressed HSCs by accelerating oxidative DNA damage repair. Innovations and Conclusion: Our findings reveal the action of mechanism for Salidroside in PARP1 stimulation and a novel role of PARP1 activation in maintaining HSC function under oxidative stress. Antioxid. Redox Signal. 20, 1853–1865.

Salidroside Reduces Cell Mobility via NF-κB and MAPK Signaling in LPS-Induced BV2 Microglial Cells

Abstract: The unregulated activation of microglia following stroke results in the production of toxic factors that propagate secondary neuronal injury. Salidroside has been shown to exhibit protective effects against neuronal death induced by different insults. However, the molecular mechanisms responsible for the anti-inflammatory activity of salidroside have not been elucidated clearly in microglia. In the present study, we investigated the molecular mechanism underlying inhibiting LPS-stimulated BV2 microglial cell mobility of salidroside. The protective effect of salidroside was investigated in microglial BV2 cell, subjected to stretch injury. Moreover, transwell migration assay demonstrated that salidroside significantly reduced cell motility. Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells. Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF-κB) by blocking degradation of IκBα and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression. These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.

Rhodiola rosea L. extract and its active compound salidroside antagonized both induction and reinstatement of nicotine place preference in mice

Abstract: Rationale Conventional pharmacological treatments for drug addiction aim to reduce three most important aspects: withdrawal syndrome, craving, and relapse. Pharmacological treatments currently available for the treatment of tobacco smoking are able to alleviate withdrawal symptoms but are not sufficiently effective in reducing craving and rarely effective to prevent relapse. Rhodiola rosea L., a well-known traditional oriental medicine with anxiolytic, antidepressive, antistress, and adaptogenic properties, has been recently shown to be effective in the prevention and treatment of nicotine-withdrawal symptoms.

Pretreatment with 2-(4-methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-D-pyranoside attenuates cerebral ischemia/reperfusion-induced injury in vitro and in vivo.

Abstract: Salidroside, extracted from the root of Rhodiola rosea L, is known for its pharmacological properties, in particular its neuroprotective effects. 2-(4-Methoxyphenyl) ethyl-2-acetamido-2-deoxy-β-D- pyranoside (GlcNAc-Sal), an analog of salidroside, was recently synthesized and shown to possess neuroprotective properties. The purpose of the current study was to investigate the neuroprotective effects of GlcNAc-Sal against oxygen–glucose deprivation-reperfusion (OGD-R)-induced neurotoxicity in vitro and global cerebral ischemia-reperfusion (GCI-R) injury in vivo. Cell viability tests and Hoechst 33342 staining confirmed that GlcNAc-Sal pretreatment markedly attenuated OGD-R induced apoptotic cell death in immortalized mouse hippocampal HT22 cells. Western blot, immunofluorescence and PCR analyses revealed that GlcNAc-Sal pretreatment restored the balance of pro- and anti-apoptotic proteins and inhibited the activation of caspase-3 and PARP induced by OGD-R treatment. Further analyses showed that GlcNAc-Sal pretreatment antagonized reactive oxygen species (ROS) generation, iNOS-derived NO production and NO-related apoptotic cell death during OGD-R stimulation. GCI-R was induced by bilateral common carotid artery occlusion (BCCAO) and reperfusion in mice in vivo. Western blot analysis showed that GlcNAc-Sal pretreatment decreased the expression of caspase-3 and increased the expression of Bcl-2 (B-cell lymphoma 2)/Bax (Bcl-2-associated X protein) induced by GCI-R treatment. Our findings suggest that GlcNAc-Sal pretreatment prevents brain ischemia reperfusion injury by the direct or indirect suppression of cell apoptosis and GlcNAc-Sal could be developed as a broad-spectrum agent for the prevention and/or treatment of cerebral ischemic injury.

Salidroside blocks the proliferation of pulmonary artery smooth muscle cells induced by platelet‑derived growth factor‑BB.

Abstract: The proliferation of pulmonary artery smooth muscle cells (PASMCs) contributes to the development of pulmonary vascular remodeling, ultimately leading to pulmonary hypertension. In this study, the effects and molecular mechanisms of salidroside on the platelet‑derived growth factor (PDGF)‑BB‑induced proliferation of primary cultured rat PASMCs were investigated. The presented data demonstrated that salidroside significantly inhibited the proliferation and DNA synthesis of PASMCs induced by PDGF‑BB in a dose‑ and time‑dependent manner, without cell cytotoxicity. In accordance with these findings, salidroside blocked progression through G0/G1 to S phase of the cell cycle. The salidroside‑induced inhibition of the cell cycle was associated with the inhibition of cyclin D1, cyclin E, cyclin‑dependent kinase 2 (CDK2) and CDK4 mRNA expression, as well as an increase in the mRNA expression of p27 in PDGF‑BB‑stimulated PASMCs. Further experiments showed that the beneficial effect of salidroside on blocking the proliferation of PASMCs was associated with the suppression of the AKT/glycogen synthase kinase 3 β (GSK3β) signaling pathway, but did not involve the extracellular signal‑regulated kinase 1/2, p38 and c‑Jun‑N‑terminal kinase signaling pathways. These results indicate that salidroside suppresses PDGF‑BB‑induced PASMC proliferation through the AKT/GSK3β signaling pathway and suggests that it may be a feasible therapy for pulmonary vascular remodeling diseases.

Analysis of five bioactive compounds from naturally occurring Rhodiola rosea in eastern Canada

Abstract: Saunders, D., Poppleton, D., Struchkov, A. and Ireland, R. 2014. Analysis of five bioactive compounds from naturally occurring Rhodiola rosea in eastern Canada. Can. J. Plant Sci. 94: 741–748. The plant Rhodiola rosea produces several bioactive compounds including salidroside, tyrosol, rosarin, rosavin, and rosin. These compounds have been used in traditional medicinal practices in Asia and are currently found in many nutraceutical mixtures. The nutraceutical qualities of these five compounds has resulted in over harvesting of natural populations of R. rosea and instigated several industrial cultivation operations. The purpose of this study was to examine R. rosea from five distinct natural populations in the maritime provinces of Canada to determine the concentrations of these five bioactive compounds. Ten samples were obtained from each of five sites and the concentration of each compound in the rhizomes was determined. Reverse phase-HPLC with a diode array detector was used to quantify the five compoun...

An LC-MS/MS method for the determination of salidroside and its metabolite p-tyrosol in rat liver tissues.

Abstract: Context: Salidroside and its metabolite p-tyrosol are two major phenols in the genus Rhodiola L. (Crassulaceae). They have been confirmed to possess various pharmacological properties and are used for the prophylaxis and therapeutics of many diseases. Several analytical methods have been developed for the determination of the two compounds in plant materials and biological plasma matrices. However, these methods are not optimal for biological samples containing complex organic interferences, such as liver and brain tissues.Objective: This study aimed to further develop and validate a simple and specific LC–MS/MS method for the determination of salidroside and its metabolite p-tyrosol in rat liver tissues using paracetamol as the internal standard (IS).Materials and methods: Salidroside and p-tyrosol with the IS paracetamol and liver tissues were used as model compounds and biological samples. Samples were processed by protein precipitation (PP) with methanol, the supernatant was dried under nitrog...

Effect of salidroside on lung injury by upregulating peroxisome proliferator‑activated receptor γ expression in septic rats

Abstract: Successful drug treatment for sepsis-related acute lung injury (ALI) remains a major clinical problem. Thus, the aim of the present study was to investigate the beneficial effects of salidroside on ameliorating cecal ligation and puncture (CLP)-induced lung inflammation. Rats underwent CLP surgery to induce ALI and 800 mg/kg salidroside (i.v.) was administered 24 h after the CLP challenge. Subsequently, biochemical changes in the blood and lung tissues, as well as morphological and histological alterations in the lungs, that were associated with inflammation and injury were analysed. CLP was shown to significantly increase the serum levels of plasma tumour necrosis factor-α and interleukin-6, -1β and-10. In addition, CLP increased pulmonary oedema, thickened the alveolar septa and caused inflammation in the lung cells. These changes were ameliorated by the administration of 800 mg/kg salidroside (i.v.) 24 h after the CLP challenge. This post-treatment drug administration also significantly attenuated the lipopolysaccharide-induced activation of nuclear factor-κβ and increased the release of peroxisome proliferator-activated receptor γ in the lung tissue. Therefore, salidroside administered following the induction of ALI by CLP significantly prevented and reversed lung tissue injuries. The positive post-treatment effects of salidroside administration indicated that salidroside may be a potential candidate for the management of lung inflammation in CLP-induced endotoxemia and septic shock.

Production of salidroside and polysaccharides in Rhodiola sachalinensis using airlift bioreactor systems

Abstract: Rhodiola sachalinensis is widely used in traditional Chinese medicine, and salidroside and polysaccharides are its important bioactive compounds This study used airlift bioreactor systems to produce mass bioactive compounds through callus culture Several factors affecting callus biomass and bioactive compound accumulation were investigated Callus growth was vigorous in a bioreactor system, and the growth ratio was 28-fold higher in bioreactor culture than in agitated-flask culture Callus biomass and polysaccharide content were favorable at 01 air volume per culture volume per min (vvm), whereas favorable salidroside content was observed at a high air volume (02 vvm) The maximum yields of salidroside (790 mg l−1) and polysaccharide (287 g l−1) were obtained at 01 vvm Inoculum density greatly affected callus biomass and bioactive compound accumulation, and the highest biomass and contents or yields of salidroside and polysaccharide were determined at a high inoculum density of 125 g l−1 The level of hydrogen ion concentration (pH) at 58 improved callus biomass accumulation Acidic medium (pH 48) stimulated salidroside synthesis but higher pH level (78) promoted polysaccharide accumulation The highest yields of both bioactive compounds were obtained at pH 58 Methyl jasmonate (MeJA) participated in synthesis promotion of bioactive compounds, and the contents and yields of salidroside [475 mg g−1 dry weight (DW), 5843 mg l−1] and polysaccharides (39241 mg g−1 DW, 479 g l−1) were at maximum at 125 and 150 μmol of MeJA Therefore, bioreactor systems can be used to produce R sachalinensis bioactive compounds, and callus culture in a bioreactor can be as an alternative method for supplying materials for commercial drug production

Ultrasonic extraction technology for salidroside in natural Rhodiola rosea

Abstract: The invention discloses an ultrasonic extraction technology for salidroside in natural Rhodiola rosea, and relates to the technical field of traditional Chinese medicine extraction. The ultrasonic extraction technology comprises the following steps: firstly, slicing salidroside; freezing, baking, freezing again, and baking again; grinding to obtain powder; adding salidroside powder into purified water at the temperature of 40-60DEG C; adding 10-15 times of water for dipping for 30 minutes; acting for 5-10min at the temperature of 50-55DEG C under the condition of ultrasonic power of 440W/L; carrying out ultrasonic extraction for three times, and combining filtrate; filtering and condensing filtrate; adding 95% alcohol of certain volume; standing for 24 hours; removing supernate; carrying out reduced pressure suction filtration; carrying out vacuum drying at the temperature of 70DEG C; drying to obtain polygahatous polysaccharide. The ultrasonic extraction technology disclosed by the invention has the advantages of short extraction time, low energy consumption, big medicinal material raw material handling capacity which is improved twofoldness or by multiple times, few impurities, low cost and obvious overall economic efficiency, and efficient ingredients can be easily separated and purified.

Inhibitory Mechanism of Salidroside on Tyrosinase

Abstract: Tyrosinase is a key rate-limiting enzyme in melanin synthesis which can be blocked to reduce melasma and freckles by inhibiting the activity of tyrosinase. Salidroside showed certain inhibitory effects on tyrosinase by enzyme kinetics with inhibition of 33.04%. Besides it was also a competitive inhibitor of tyrosinase which served as a substrate analogue to combine with enzyme to produce quinones with stronger light absorption. Furthermore, docking results implied that inhibitory mechanisms might be attributed to the weak interactions between salidroside and tyrosinase such as hydrogen bonds and van del waals. Salidroside is a main kind of plant flavonoids from Rhodiola rosea, walnut and so on. Studying inhibitory mechanism of salidroside on tyrosinase is not only helpful for developing anti-freckle products in which salidroside is one of the most important components, but also beneficial for making better use of plant flavonoids to seek for a new generation of natural skin care cosmetics.

Method for extracting salidroside from rhodiola rosea

Abstract: The invention relates to a method for extracting salidroside from rhodiola rosea. The method comprises the following treatment steps: by taking natural rhodiola rosea as a raw material, drying, grinding, allowing the rhodiola rosea to pass through a sieve with the granularity of 80 meshes, thereby obtaining rhodiola rosea powder; performing bio-enzyme enzymolysis; performing microwave assisted extraction; purifying through a macroporous resin; and crystallizing. According to the method disclosed by the invention, the rhodiola rosea is taken as the raw material, bio-enzyme enzymolysis is combined with microwave extraction, and cell walls of plants are destroyed, so that active ingredients in the cells are fully dissolved out, the extraction rate of the active ingredients is increased, and the method has the advantages of mild reaction conditions, high speed, low energy consumption, high quality, time conservation, no pollution and the like. Moreover, the microwave assisted extraction mode has the advantage that the content of protein impurities in the extracting solution is low and is suitable for industrial production.